As early as 1957 a virus was identified in children with severe diseases of the lower airway, which was designated respiratory syncytial virus (RSV). This name refers to the characteristic of the virus to cause diseases of the respiratory tract and to induce the formation of synctia in vitro.
RSV belongs to the family of paramyxoviruses and, within this, to the subfamily of the pneumoviriane. As with the other representatives of this family, RSV has a non-segmented, continuous RNA genome in negative strand orientation. The genome of the RSV is 15222 bases long and exists in complex with proteins as a nucleocapsid.
The virus genome codes a series of virus proteins. Among these are the membrane proteins, which are known as RSV G-proteins and RSV F-proteins. The G-proteins is responsible for the specific adsorption of the virus particle onto the cell surface, while the F-protein induces the fusion of the viral with the cellular membrane. The F-protein is synthesized as a precursor polypeptide F0 and has on the N-terminal end, a signal peptide for the transport of the translocation complex to the membrane of the endoplasmic reticulum. After the amino acid chain is fed through the membrane, a hydrophobic sequence at the C-terminal end effects the anchoring of the F0 protein in the membrane and the signal peptide is cleaved off. Following this, the protein is glycosylated during its transport through the Golgi apparatus. A cleavage of the F0 protein into the amino terminal F2 part and the F1 protein also takes place in the Golgi apparatus. The cleavage site lies between a segment of basic amino acids and a hydrophobic domain. This hydrophobic domain of about 25 amino acids in length forms, after the cleavage, the N-terminus of the F1 protein and mediates the merging of the viral with the cellular membrane following absorption. The F2 protein remains connected to the F1 protein via a disulfide bridge.
Antibodies directed against this fusion-mediating peptide of the F1 protein can prevent the virus from being taken up into the cell and thus have a neutralizing effect.
Infection with RSV is highly contagious; in a milliliter of saliva there exist up to 106 infectious virus particles. It is transmitted primarily by droplet and direct contact with infected persons. Especially children become infected during the winter months.
RSV is considered the main infectological problem of the first year of life. Infants in the age between six weeks and a half year are especially in danger. At the age of four years, 80% of children have antibodies against the virus.
However, reinfections with mild forms of the disease also develop in later age as a result of a reduced antibody concentration. Especially frequent are noskomial infections in convalescent homes, kindergartens and -clinics.
The incubation time of RSV is approximately 4-5 days. The disease presents with mild to severe life threatening influenzal infections with fever and sniffles. Infections of the throat (pharyngitis) and the trachea (tracheitis) as well as of the bronchiae (bronchitis) are also commonly observed.
Following the droplet infection of the upper respiratory tract, the virus reproduces in the cells of the mucous membranes and, from there, can spread into the lower air passages within one to two days.
A vaccine against RSV is not presently known. Viruses killed by formalin were minimally successful, since the F-protein is destroyed by the chemical treatment and only antibodies against the G-protein are formed. While these are virus-neutralizing, they cannot however prevent the spread of the virus by cell fusions. Although a passive immunization by giving immunoglobulins is used, it is associated with high costs and is thus unsuitable for the prophylactic immunization of larger population groups.
There thus continues to exist a need for an effective vaccine against an infection with RSV.